As alkanoic acid derivatives, the compounds described in the following references are known.    (1) WO 00/64876 describes, as a PPAR ligand-receptor binder, a compound represented by the formula:
wherein
are each independently an aryl and the like; A is —O— and the like; B is —O— and the like; D is —O— and the like; E is a bond or an ethylene group; a, b, c and e are each 0–4; d is 0–5; f is 0–6; R1, R3, R5, R7, R9 and R11, are each independently a hydrogen and the like; R2, R4, R6, R8, R10 and R12 are each independently —(CH)q—X; q is 0–3; X is hydrogen and the like; Z is R21O2C— and the like; R21 is hydrogen and the like.    (2) WO 92/20350 describes, as a substance capable of mimicking the action of physiologically active natural polymer, a compound represented by the formula: Mi—(Mn)n—Mt wherein n is the number of 2 to about 50; Mi, Mn and Mt are
respectively;wherein
are each independently an aromatic carbocycle or an aromatic heterocycle; Ai, Bi, An, Bn, At, Bt, Ti and Tt are each independently hydrogen or a substituent; and Xi and Xn are each independently a bond and the like.    (3) JP-A-4-217668 describes, as an antibacterial agent for agriculture and horticulture and an intermediate therefor, compounds respectively represented by the formula:
and the formula:
wherein R1 and R2 are each independently a hydrogen atom or a C1–C5 alkyl group, A is
wherein X is a C1–C10 alkyl group optionally having one or more substituents selected from a C1–C5 alkoxy group, a halogen atom, a nitro group, a cyano group and a trifluoromethyl group and the like and B is a methoxycarbonyl group or a cyano group.
Peroxisome proliferator-activated receptor gamma (PPARγ), a member of the intranuclear hormone receptor superfamily, which is typically exemplified by steroid hormone receptors and thyroid hormone receptors, plays an important role as a master regulator in the differentiation of adipocytes with its expression induced in the very early stage of adipocyte differentiation. PPARγ forms a dimer with the retinoid X receptor (RXR) by binding to a ligand, and binds to a responsive site of the target gene in the nucleus to directly control (activate) transcription efficiency. In recent years, the possibility that 15-deoxy-Δ12.14 prostaglandin J2, which is a metabolite of prostaglandin D2, serves as an endogenous ligand for PPARγ, has been suggested, and it has been shown that a class of insulin resistance enhancers, typically exemplified by thiazolidinedione derivatives, possess ligand activity for PPARγ, and that its potency is proportional to its hypoglycemic action or adipocyte differentiation-promoting action [Cell, vol. 83, p. 803 (1995): The Journal of Biological Chemistry, vol. 270, p. 12953 (1995); Journal of Medicinal Chemistry, vol. 39, p. 655 (1996)]. Furthermore, in recent years, it has been shown that 1) PPARγ is expressed in cultured cells of human liposarcoma origin, whose proliferation is ceased by the addition of a PPARγ ligand [Proceedings of the National Academy of Sciences of the United States of America, vol. 94, p. 237 (1997)], 2) nonsteroidal anti-inflammatory drugs, typically exemplified by indomethacin and fenoprofen, have PPARγ ligand activity [The Journal of Biological Chemistry, vol. 272, p. 3406 (1997)], 3) PPARγ is expressed at high levels in activated macrophages, with the transcription of a gene involved in inflammation inhibited by the addition of a ligand therefor [Nature, vol. 391, p. 79 (1998)], and 4) PPARγ ligands suppress the production of inflammatory cytokines (TNFα, IL-1β, IL-6) by monocytes [Nature, vol. 391, p. 82 (1998)].